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The podoplanin-CLEC-2 axis inhibits inflammation in sepsis
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Journal Article
The podoplanin-CLEC-2 axis inhibits inflammation in sepsis
2017
Overview
Platelets play a critical role in vascular inflammation through the podoplanin and collagen/fibrin receptors, C-type-lectin-like-2 (CLEC-2) and glycoprotein VI (GPVI), respectively. Both receptors regulate endothelial permeability and prevent peri-vascular bleeding in inflammation. Here we show that platelet-specific deletion of CLEC-2 but not GPVI leads to enhanced systemic inflammation and accelerated organ injury in two mouse models of sepsis–intra-peritoneal lipopolysaccharide and cecal ligation and puncture. CLEC-2 deficiency is associated with reduced numbers of podoplanin-expressing macrophages despite increased cytokine and chemokine levels in the infected peritoneum. Pharmacological inhibition of the interaction between CLEC-2 and podoplanin regulates immune cell infiltration and the inflammatory reaction during sepsis, suggesting that activation of podoplanin underlies the anti-inflammatory action of platelet CLEC-2. We suggest podoplanin-CLEC-2 as a novel anti-inflammatory axis regulating immune cell recruitment and activation in sepsis.
Sepsis is a life-threatening condition where exaggerated inflammatory responses lead to severe tissue damage. Here, Rayes and colleagues show that the interaction between podoplanin and its receptor CLEC-2 on platelets plays a critical role in limiting inflammation during sepsis.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 64
/ 64/60
/ Animals
/ Bleeding
/ Blood Platelets - immunology
/ Cecum
/ Collagen
/ Fibrin
/ Humanities and Social Sciences
/ Lectins, C-Type - immunology
/ Ligation
/ Lipopolysaccharides - toxicity
/ Membrane Glycoproteins - genetics
/ Membrane Glycoproteins - immunology
/ Mice
/ Multiple Organ Failure - immunology
/ Platelet Membrane Glycoproteins - genetics
/ Platelet Membrane Glycoproteins - immunology
/ Rodents
/ Science
/ Sepsis
